Single Drug Treatment for Alzheimer's, MS, TBI, and More

In a study published in the Journal of Neuroscience, a collaborative team of researchers led by Linda J. Van Eldik, director of the University of Kentucky Sanders-Brown Center on Aging, and D. Martin Watterson of the Northwestern University Feinberg School of Medicine, present results showing that a new central nervous system drug compound can reduce Alzheimer’s pathology in a mouse model of the disease.

The drug, called MW-151, is a selective suppressor of brain inflammation and overproduction of pro-inflammatory molecules from glial cells. The drug can be taken by mouth and readily enters the brain. The new study tested the hypothesis that intervention with drugs like MW-151 could be effective as a preventive measure, when administered at an early stage before Alzheimer's pathology appears, as well as after disease symptoms have begun to appear. _Source

The UK / Northwestern team has developed two drugs in this new class -- MW 151 and MW 189. This new class of drugs protects the brain by limiting production of and preventing the accumulation of pro-inflammatory cytokines in the brain. Inflammation in the brain can be particularly destructive in a wide range of infections, diseases, traumatic injuries, vascular insufficiencies, and more.

When too many of the cytokines are produced, the synapses of the brain begin to misfire. Eventually the entire organization of the brain falls into disarray, like a computer failing. The neurons lose their connections with each other and can eventually die. The resulting damage in the cortex and hippocampus can compromise memory and decision-making.

"In Alzheimer's disease, many people now view the progression from mild cognitive impairment to full-blown Alzheimer's as an indication of malfunctioning synapses, the pathways that allow neurons to talk to each other," said Watterson, the John G. Searle Professor of Molecular Biology and Biochemistry. "And high levels of proinflammatory cytokines can contribute to synaptic malfunction."

Because this harmful inflammatory mechanism also appears to be a major player in other neurodegenerative disorders in addition to Alzheimer's, the class of drugs represented by MW151 might hold bright potential as co-therapies for Parkinson's disease, frontotemporal dementia, amyotrophic lateral sclerosis, M.S. and the longer term complications of brain injury, Watterson said. _MedXpress

It is likely that this new class of drugs with its very broad spectrum of affects will find application in a wide range of conditions -- some not yet anticipated.

Regardless of neuro-inflammation’s exact role, a prevailing hypothesis is that targeting of pro-inflammatory cytokine overproduction in the brain might be a useful therapeutic strategy to add to the armamentarium of emerging interventions. The primary brain cell target for such a disease modifying strategy would be glia, cells in the brain that produce pro-inflammatory cytokines and other innate immunity responses to injury or disease progression. Glial cells normally cooperate with the nerve cells to keep the brain operating smoothly. When an injury or change in the brain occurs, the glial cells mount a beneficial inflammation response to fight off the insult and restore the brain to its proper functioning. This beneficial process sometimes gets out of balance and the inflammation becomes too strong or does not shut off on schedule. _SurfKy